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Engineering Approach to the Ventilatory Pump

呼吸泵的工程方法

基本信息

批准号：
7256228
负责人：
Aladin M Boriek
金额：
$ 32.11万
依托单位：
BAYLOR COLLEGE OF MEDICINE
依托单位国家：
美国
项目类别：
财政年份：
2004
资助国家：
美国
起止时间：
2004-08-01 至 2009-07-31
项目状态：
已结题

来源：
https://reporter.nih.gov/project-details/7256228
关键词：
Breathing Canis familiaris Cause of Death Chest wall structure Chronic Chronic Obstructive Airway Disease Clinical Complement Condition Data Disease Electron Beam Tomography Engineering Evaluation Failure Fluoroscopy Frequencies Goals Health Human Individual Knowledge Lung Lung diseases Lung volume reduction surgery Measures Mechanics Mediating Membrane Modeling Morbidity - disease rate Motion Muscle Muscle Contraction Muscle Fibers Muscle function Operative Surgical Procedures Patients Property Publishing Pulmonary Emphysema Pump Rate Relative (related person)Respiratory Diaphragm Respiratory Failure Scanning Shapes Slice Speed Staging Stress Structural Models Structure Techniques Testing Total Lung Capacity base cost expiration functional restoration human subject improved in vivo interest kinematics lung volume mathematical model membrane model mortality pressure productivity loss programs respiratory rib bone structure theories

项目摘要

DESCRIPTION (provided by applicant): Respiratory failure is a major cause of morbidity and mortality in patients with chronic obstructive pulmonary disease (COPD). However, the mechanical determinants of ventilatory pump function are still not well understood. Our goal is to use an engineering approach to investigate the mechanical factors that mediate pump failure in COPD. Hyperinflation of the lungs and extreme diaphragm shortening can distort the sheet of the diaphragm, cause loss of its membrane curvature, and reduce its muscle force. This will severely limit the function of the ventilatory pump. Our objective is to build a general model of diaphragm mechanics that can be utilized to evaluate the effect of lung volume reduction surgery on respiratory pump function in patients with severe emphysema. We will extend our knowledge of diaphragm and chest wall mechanics in dogs, and will begin to apply the same principles and approaches to the study of ventilatory mechanics in normal human subjects and patients with severe emphysema before and after lung volume reduction surgery (LVRS). Finally, we will develop a comprehensive theory of diaphragm mechanics that can eventually be used to predict diaphragm muscle function in both healthy and diseased states. We will achieve this objective with in vivo studies of diaphragm mechanics in dogs and humans complemented with mathematical modeling techniques. Our specific aims are: Specific Aim #1: To determine how hyperinflation of the lungs alters the pressure generating ability of the diaphragm during simultaneous sub-maximal and maximal activation of both hemi-diaphragms. Hypothesis 1: Extreme muscle contraction of both hemi-diaphragms at high frequencies of stimulation and at lower lung volumes causes flattening and distortion of the membrane of the diaphragm, and therefore its generating ability of pressure is severely compromised. Specific Aim #2: To develop a comprehensive mechanical model of the diaphragm. Hypothesis 3: A comprehensive mechanical model of the diaphragm that utilizes both structure and constitutive relationships of the diaphragm should provide sufficient quantitative information on the evaluation of the pressure generating ability of the ventilatory pump. Specific Aim #3: To evaluate diaphragm function in patients with end-stage emphysema before and after LVRS, and in normal humans. Hypothesis 2a: In normal individuals, muscle fibers are oriented along the direction of maximum principal curvature, Hypothesis 2b: In severe emphysema patients, the diaphragm is comparatively flattened, and after LVRS, there is a gain in diaphragm muscle fiber curvature. Therefore, membrane tension is transmitted into trans-diaphragmatic pressure more effectively than before the surgery. Once we obtained the distribution of principal curvatures we will use our model of diaphragm mechanics developed in Aim 2 to predict diaphragm function in normal individuals and patients with severe emphysema before and after LVRS. The completion of these aims will significantly enhance our fundamental understanding of the ventilatory pump function in health and disease.

描述（由申请人提供）：呼吸衰竭是慢性阻塞性肺疾病（COPD）患者发病和死亡的主要原因。然而，通气泵功能的机械决定因素仍未得到很好的理解。我们的目标是使用工程方法来研究介导COPD中泵失效的机械因素。肺的过度膨胀和横膈膜的极度缩短会使横膈膜扭曲，导致其膜曲率的丧失，并减少其肌肉力量。这将严重限制通风泵的功能。我们的目的是建立一个通用的隔膜力学模型，用于评估肺减容手术对严重肺气肿患者呼吸泵功能的影响。我们将扩展我们对狗的隔膜和胸壁力学的知识，并将开始将相同的原理和方法应用于正常人和肺减容手术（LVRS）前后严重肺气肿患者的通气力学研究。最后，我们将发展一个全面的隔膜力学理论，最终可用于预测健康和患病状态下隔膜肌的功能。我们将通过对狗和人的隔膜力学进行体内研究，并辅以数学建模技术来实现这一目标。我们的具体目标是：具体目标#1：确定在同时激活半膈肌的亚最大和最大时，肺部的过度膨胀如何改变膈肌的压力产生能力。假设1：在高频率刺激和低肺容量时，半膈肌的极度肌肉收缩导致膈膜变平和扭曲，因此其产生压力的能力严重受损。具体目标2：建立隔膜的综合力学模型。假设3：综合利用隔膜的结构和本构关系的隔膜力学模型应该能为评价通风泵的压力产生能力提供足够的定量信息。具体目的#3：评估LVRS前后终末期肺气肿患者和正常人的膈肌功能。假设2a：正常人肌纤维沿最大主曲率方向排列，假设2b：严重肺气肿患者膈肌相对扁平，LVRS后膈肌肌纤维弯曲增加。因此，膜张力比术前更有效地传递为横膈膜压力。一旦我们获得主曲率的分布，我们将使用Aim 2中开发的隔膜力学模型来预测正常人和LVRS前后严重肺气肿患者的隔膜功能。这些目标的完成将大大提高我们对呼吸泵在健康和疾病中的功能的基本理解。